The Behavioral Neuroscience of Eating

Clinical syndromes stimulate basic science by providing unexpected combinations or dissociations of phenomena that basic science did not predict or cannot explain. That clinical eating disorders in which abnormally large meals can occur in patients with low, normal, or high body weight contradicts the assumption that the only function of eating is to provide energy intake for nutritional homeostasis. In the past decade the basic science of eating has responded to this problem in such a fundamental way that it has undergone a paradigm shift. Instead of seeking the neurobiological mechanisms of eating solely in the molecular transformations of energy homeostasis, eating is now seen as a problem in behavioral neuroscience. This shift promises for the first time an adequate basic science of eating because the new view includes genetic and sexual vulnerabilities, learning, and a coherent neural system composed of peripheral feedbacks and central integrations that use amines, peptides, and steroids. The shift has been driven by the recent progress in a ‘‘top-down’’ analysis of meals, the functional unit of eating (1). This analysis has included the application of molecular genetics that revealed a central cascade of neuropeptides, the recognition that the neurology of eating was a system that integrated peripheral feedback and central information to turn a central pattern generator for oromotor movements on and off, the realization that learned controls of eating developed rapidly and acted frequently, and a renewed attack on the mechanisms by which estrogen inhibits eating. We review these areas in this chapter.